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本文引用的文献

1
The fructose-fed rat: a review on the mechanisms of fructose-induced insulin resistance and hypertension.果糖喂养大鼠:果糖诱导胰岛素抵抗和高血压的机制综述。
Mol Cell Biochem. 2009 Dec;332(1-2):145-59. doi: 10.1007/s11010-009-0184-4. Epub 2009 Jun 18.
2
Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.摄入果糖甜味而非葡萄糖甜味的饮料会增加超重/肥胖人群的内脏脂肪和血脂,并降低胰岛素敏感性。
J Clin Invest. 2009 May;119(5):1322-34. doi: 10.1172/JCI37385. Epub 2009 Apr 20.
3
Ketohexokinase-dependent metabolism of fructose induces proinflammatory mediators in proximal tubular cells.果糖的酮己糖激酶依赖性代谢在近端肾小管细胞中诱导促炎介质。
J Am Soc Nephrol. 2009 Mar;20(3):545-53. doi: 10.1681/ASN.2008060576. Epub 2009 Jan 21.
4
Endothelin-1 modulates angiotensin II in the development of hypertension in fructose-fed rats.内皮素-1在果糖喂养大鼠高血压发展过程中调节血管紧张素II。
Mol Cell Biochem. 2009 May;325(1-2):89-97. doi: 10.1007/s11010-008-0023-z. Epub 2009 Jan 13.
5
Activation of ATP-sensitive potassium channels protects vascular endothelial cells from hypertension and renal injury induced by hyperuricemia.ATP敏感性钾通道的激活可保护血管内皮细胞免受高尿酸血症诱导的高血压和肾损伤。
J Hypertens. 2008 Dec;26(12):2326-38. doi: 10.1097/HJH.0b013e328312c8c1.
6
Uric acid stimulates endothelin-1 gene expression associated with NADPH oxidase in human aortic smooth muscle cells.尿酸刺激人主动脉平滑肌细胞中与NADPH氧化酶相关的内皮素-1基因表达。
Acta Pharmacol Sin. 2008 Nov;29(11):1301-12. doi: 10.1111/j.1745-7254.2008.00877.x.
7
Uric acid activates extracellular signal-regulated kinases and thereafter endothelin-1 expression in rat cardiac fibroblasts.尿酸激活细胞外信号调节激酶,进而促进大鼠心肌成纤维细胞内皮素-1 的表达。
Int J Cardiol. 2010 Feb 18;139(1):42-9. doi: 10.1016/j.ijcard.2008.09.004. Epub 2008 Oct 21.
8
Validation of simple indexes to assess insulin sensitivity during pregnancy in Wistar and Sprague-Dawley rats.评估Wistar和Sprague-Dawley大鼠孕期胰岛素敏感性的简单指标的验证
Am J Physiol Endocrinol Metab. 2008 Nov;295(5):E1269-76. doi: 10.1152/ajpendo.90207.2008. Epub 2008 Sep 16.
9
Uric acid decreases NO production and increases arginase activity in cultured pulmonary artery endothelial cells.尿酸可降低培养的肺动脉内皮细胞中一氧化氮的生成,并增加精氨酸酶活性。
Am J Physiol Cell Physiol. 2008 Nov;295(5):C1183-90. doi: 10.1152/ajpcell.00075.2008. Epub 2008 Sep 10.
10
Effect of allopurinol on blood pressure of adolescents with newly diagnosed essential hypertension: a randomized trial.别嘌醇对新诊断原发性高血压青少年血压的影响:一项随机试验。
JAMA. 2008 Aug 27;300(8):924-32. doi: 10.1001/jama.300.8.924.

卡托普利和别嘌醇联合延缓果糖诱导的代谢综合征。

Combination of captopril and allopurinol retards fructose-induced metabolic syndrome.

机构信息

Division of Renal Diseases and Hypertension, University of Colorado, Denver, Colo., USA.

出版信息

Am J Nephrol. 2009;30(5):399-404. doi: 10.1159/000235731. Epub 2009 Aug 21.

DOI:10.1159/000235731
PMID:19696478
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2783362/
Abstract

BACKGROUND

Both ACE inhibitors and allopurinol have been shown to partially prevent metabolic syndrome induced by fructose. We tested the hypothesis that combined therapy might be more effective at blocking the metabolic syndrome induced with fructose.

METHODS

Male Sprague-Dawley rats were fed a high fructose diet with or without allopurinol, captopril, or the combination for 20 weeks. A control group received a normal diet. All groups were pair-fed to assure equivalent caloric intake.

RESULTS

Despite reduced energy intake, the fructose-fed rats developed features of metabolic syndrome including elevated blood pressure, abdominal obesity, hypertriglyceridemia, hyperuricemia and hyperinsulinemia. While both allopurinol and captopril alone tended to reduce features of the metabolic syndrome, the combined therapy was synergistic, with significant reduction in blood pressure, less accumulation of abdominal fat, an improvement in the dyslipidemia and a complete prevention of insulin resistance.

CONCLUSION

A high fructose diet can induce metabolic syndrome even in the setting of caloric restriction. Captopril and allopurinol synergistically reduce features of the metabolic syndrome, especially hypertension, insulin resistance and dyslipidemia. Combination allopurinol and ACE inhibitor therapy might provide a superior means to prevent diabetes and cardiovascular disease.

摘要

背景

血管紧张素转换酶抑制剂和别嘌呤醇都已被证明可以部分预防果糖引起的代谢综合征。我们检验了这样一种假设,即联合治疗可能更有效地阻止果糖引起的代谢综合征。

方法

雄性 Sprague-Dawley 大鼠用高果糖饮食喂养,同时给予别嘌呤醇、卡托普利或两者联合治疗 20 周。对照组给予正常饮食。所有组均进行配对喂养,以确保摄入等量的热量。

结果

尽管能量摄入减少,果糖喂养的大鼠仍出现代谢综合征的特征,包括血压升高、腹部肥胖、高三酰甘油血症、高尿酸血症和高胰岛素血症。虽然别嘌呤醇和卡托普利单独治疗都倾向于减轻代谢综合征的特征,但联合治疗具有协同作用,可显著降低血压、减少腹部脂肪堆积、改善血脂异常并完全预防胰岛素抵抗。

结论

即使在热量限制的情况下,高果糖饮食也可诱导代谢综合征。卡托普利和别嘌呤醇协同减轻代谢综合征的特征,特别是高血压、胰岛素抵抗和血脂异常。联合应用别嘌呤醇和 ACE 抑制剂治疗可能是预防糖尿病和心血管疾病的更好方法。